Hepatitis

Hepatitis describes inflammation in the liver. This can vary from a chronic low level inflammation to acute and severe inflammation that leads to large areas of necrosis and liver failure.

Causes

  • Alcoholic hepatitis
  • Non alcoholic fatty liver disease
  • Viral hepatitis
  • Autoimmune hepatitis
  • Drug induced hepatitis (e.g. paracetamol overdose)

 

Presentation

Hepatitis may be asymptomatic or could present with non-specific symptoms:

  • Abdominal pain
  • Fatigue
  • Pruritis (itching)
  • Muscle and joint aches
  • Nausea and vomiting
  • Jaundice
  • Fever (viral hepatitis)

Typical biochemical findings are that liver function tests become deranged with high transaminases (AST / ALT) with proportionally less of a rise in ALP. This is referred to as a “hepatitic picture”. Transaminases are liver enzymes that are released into the blood as a result of inflammation of the liver cells. Bilirubin can also rise as a result of inflammation of the liver cells. High bilirubin causes jaundice.

 

Hepatitis A

Hepatitis A is the most common viral hepatitis worldwide but it is relatively rare in the UK with under 1000 cases in England and Wales in 2017. It is an RNA virus. It is transmitted via the faecal-oral route usually by contaminated water or food. It presents with nausea, vomiting, anorexia and jaundice. It can cause cholestasis (slowing of bile flow through the biliary system) with dark urine and pale stools and moderate hepatomegaly. It resolves without treatment in around 1-3 months. Management is with basic analgesia. Vaccination is available to reduce the chance of developing the infection. It is a notifiable disease and Public Health need to be notified of all cases.

 

Hepatitis B

Hepatitis B is a DNA virus. It is transmitted by direct contact with blood or bodily fluids, such as during sexual intercourse or sharing needles (i.e. IV drug users or tattoos). It can also be passed through sharing contaminated household products such as toothbrushes or contact between minor cuts or abrasions. It can also be passed from mother to child during pregnancy and delivery (known as “vertical transmission”).

Most people fully recover from the infection within 2 months, however 10% go on to become chronic hepatitis B carriers. In these patients the virus DNA has integrated into their own DNA and so they will continue to produce the viral proteins.

 

Viral markers:

Remember that antibodies are produced by the immune system against pathogen proteins. Antigens are proteins that are targeted by the antibodies, in this scenario they are part of the virus.

  • Surface antigen (HBsAg) – active infection
  • E antigen (HBeAg) – marker of viral replication and implies high infectivity
  • Core antibodies (HBcAb) – implies past or current infection
  • Surface antibody (HBsAb) – implies vaccination or past or current infection
  • Hepatitis B virus DNA (HBV DNA) – this is a direct count of the viral load

When screening for hepatitis B, test HBcAb (for previous infection) and HBsAg (for active infection). If these are positive then do further testing for HBeAg and viral load.

HBsAb demonstrates an immune response to HBsAg. The HBsAg is given in the vaccine, so having a positive HBsAb may simply indicate they have been vaccinated and created an immune response to the vaccine. The HBsAb may also be present in response to an infection. The other viral markers are necessary to distinguish between previous vaccination or infection.

Hepatitis B c antibodies (HBcAb) can help distinguish acute, chronic and past infections. We can measure IgM and IgG versions of the HBcAb. IgM implies an active infection and will give a high titre with an acute infection and a low titre with a chronic infection. IgG indicates a past infection where the HBsAg is negative.

Hepatitis B e antigen (HBeAg) is important. Where the HBeAg is present it implies the patient is in an acute phase of the infection where the virus is actively replicating. The level of HBeAg correlates with their infectivity. If the HBeAg is higher, they are highly infectious to others. When they HBeAg is negative but the hepatitis B e antibody is positive this implies they have been through a phase where the virus was replicating and but the virus has now stopped replicating and they are less infectious.

Vaccination:

Vaccination is available and involves injecting the hepatitis B surface antigen. Vaccinated patients are tested for HBsAb to confirm their response to the vaccine. The vaccine requires 3 doses at different intervals. Vaccination to hep B is now included as part of the UK routine vaccination schedule (as part of the 6 in 1 vaccine).

 

Management:

  • Have a low threshold for screening patients that are at risk of hepatitis B.
  • Screen for other blood born viruses (hepatitis A and B and HIV) and other sexually transmitted diseases
  • Refer to gastroenterology, hepatology or infectious diseases for specialist management
  • Notify Public Health (it is a notifiable disease)
  • Stop smoking and alcohol
  • Education about reducing transmission and informing potential at risk contacts
  • Testing for complications: FibroScan for cirrhosis and ultrasound for hepatocellular carcinoma
  • Antiviral medication can be used to slow the progression of the disease and reduce infectivity
  • Liver transplantation for end-stage liver disease

 

Hepatitis C

Hepatitis C is an RNA virus. It is spread by blood and body fluids. No vaccine is available. It is now curable with direct acting antiviral medications.

 

Disease Course

  • 1 in 4 fights off the virus and makes a full recovery
  • 3 in 4 it becomes chronic
  • Complications: liver cirrhosis and associated complications and hepatocellular carcinoma

 

Testing

  • Hepatitis C antibody is the screening test
  • Hepatitis C RNA testing is used to confirm the diagnosis of hepatitis C, calculate viral load and assess for the individual genotype

 

Management

  • Have a low threshold for screening patients that are at risk of hepatitis C
  • Screen for other blood born viruses (hepatitis A and B and HIV) and other sexually transmitted diseases
  • Refer to gastroenterology, hepatology or infectious diseases for specialist management
  • Notify Public Health (it is a notifiable disease)
  • Stop smoking and alcohol
  • Education about reducing transmission and informing potential at risk contacts
  • Testing for complications: FibroScan for cirrhosis and ultrasound for hepatocellular carcinoma
  • Antiviral treatment with direct acting antivirals (DAAs) is tailored to the specific viral genotype. They successfully cure the infection in over 90% of patients. They are typically taken for 8 to 12 weeks
  • Liver transplantation for end-stage liver disease

 

Hepatitis D

Hepatitis D is an RNA virus. It can only survive in patients who also have a hepatitis B infection. It attaches itself to the HBsAg to survive and cannot survive without this protein. There are very low rates in the UK. Hepatitis D increases the complications and disease severity of hepatitis B. There is no specific treatment for hepatitis D. It is a notifiable disease and Public Health need to be notified of all cases.

 

Hepatitis E

Hepatitis E is an RNA virus. It is transmitted by the faecal oral route. It is very rare in the UK. Normally it produces only a mild illness, the virus is cleared within a month and no treatment is required. Rarely it can progress to chronic hepatitis and liver failure, more so in patients that are immunocompromised. There is no vaccination. It is a notifiable disease and Public Health need to be notified of all cases.

 

Autoimmune hepatitis

Autoimmune hepatitis is a rare cause of chronic hepatitis. We are not sure of the exact cause, however it could be associated with a genetic predisposition and triggered by environmental factors such as a viral infection that causes a T cell-mediated response against the liver cells. This is where the T cells of the immune system recognise the liver cells as being harmful and alert the rest of the immune system to attack these cells.

There are two types that have different ages of onset and autoantibodies:

  • Type 1: occurs in adults
  • Type 2: occurs in children

Type 1 typically affects women in their late forties or fifties. It presents around or after the menopause with fatigue and features of liver disease on examination. It takes a less acute course than type 2.

In type 2, patients in their teenage or early twenties present with acute hepatitis with high transaminases and jaundice.

Investigations will show raised transaminases (ALT and AST), IgG levels and it is associated with many autoantibodies.

 

Type 1 Autoantibodies:

  • Anti-nuclear antibodies (ANA)
  • Anti-smooth muscle antibodies (anti-actin)
  • Anti-soluble liver antigen (anti-SLA/LP)

 

Type 2 Autoantibodies:

  • Anti-liver kidney microsomes-1 (anti-LKM1)
  • Anti-liver cytosol antigen type 1 (anti-LC1)

 

Diagnosis can be confirmed using a liver biopsy.

 

Treatment is with high dose steroids (prednisolone) that are tapered over time as other immunosuppressants, particularly azathioprine, are introduced. Immunosuppressant treatment is usually successful in inducing remission however it is usually required life long. Liver transplant may be required in end stage liver disease, however the autoimmune hepatitis can recur in transplanted livers.

 

Last updated January 2019
WordPress Theme built by Shufflehound. Copyright 2016-2021 - Zero to Finals - All Rights Reserved